A role for retinoic acid in homeostatic plasticity.
Prolonged changes in neuronal activity trigger compensatory modifications in synaptic function to restore firing rates to normal levels. In this issue of Neuron, Aoto et al. demonstrate that synthesis of retinoic acid offsets chronic network inactivity by increasing synaptic strength through upregulation of GluR1 receptors.
Groth
Rachel D
RD
Department of Molecular and Cellular Physiology, Stanford University, Stanford, CA 94305, USA. rgroth@stanford.edu
Tsien
Richard W
RW
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D001921:Brain / Q000378:metabolism*; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D009415:Nerve Net / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D009474:Neurons / Q000378:metabolism*; D018091:Receptors, AMPA / Q000378:metabolism; D009435:Synaptic Transmission / Q000502:physiology*; D014212:Tretinoin / Q000502:physiology*
D018091:Receptors, AMPA; D014212:Tretinoin